Differential Risk: Gender and Racial Differences in the Relationship between Trauma, Discrimination, and Schizotypy.

Traumatic experiences are associated with increased experiences of positive schizotypy. This may be especially important for People of Color, who experience higher rates of trauma and racial discrimination. No study to date has examined how racial disparities in traumatic experiences may impact schizotypy. Furthermore, of the studies that have examined the relationship between trauma and schizotypy, none have examined racial discrimination as a potential moderator. The present study examined if racial discrimination moderates the relationship between trauma and multidimensional (positive, negative, and disorganized) schizotypy. In a sample of 770 college students, we conducted chi-squared analyses, analyses of variance, and stepwise regressions. We found that Black students experienced significantly higher racial discrimination and trauma than Latinx and Asian students. Furthermore, Black and Latinx students experienced significantly more multidimensional schizotypy items than Asian students. Trauma and racial discrimination explained 8 to 23% of the variance in each dimension of schizotypy. Racial discrimination did not moderate the relationships between trauma and multidimensional schizotypy. Our findings suggest that we need to examine risk factors that may prevent recovery from psychotic disorders. Additionally, disorganized schizotypy showed the most robust associations and may be a critical site of intervention.

Shifting the gaze from racism to healing from racism: A systematic review of selected psychology journals from 1992 to 2022.

Using a decolonial approach, we provided a narrative review of the research on racism in psychology and conducted a systematic review of the top five psychology journals publishing research on racism and mental health to identify trends in racism research over time and the research gaps. We examined 372 articles on racism published between 1992 and 2022: American Psychologist, Cultural Diversity and Ethnic Minority Psychology, Journal of Black Psychology, Journal of Counseling Psychology, and The Counseling Psychologist. Based on our review, we found that published research examining racism has steadily increased over the past 3 decades, with the greatest spikes in 2021 and 2022. The largest increase was in studies focused on People of Color's experiences with racism. The overwhelming majority of the articles were empirical (86.3%) and most of these studies (87.5%) employed cross-sectional designs. We identified corollary topics by racial/ethnic group, prevalent research designs, and the emergence of strength-based and healing approaches to address racism's impact. There were general racial and ethnic differences in trends, with research on various People of Color groups focused on the harmful effects of racism and research on White populations focused on Whiteness and level of awareness of racism. We conclude with recommendations to enhance the content and methodological rigor of future research while also suggesting policy implications to support advancements in this critical area of study. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

The neuroanatomy of developmental language disorder: a systematic review and meta-analysis.

Developmental language disorder (DLD) is a common neurodevelopmental disorder with adverse impacts that continue into adulthood. However, its neural bases remain unclear. Here we address this gap by systematically identifying and quantitatively synthesizing neuroanatomical studies of DLD using co-localization likelihood estimation, a recently developed neuroanatomical meta-analytic technique. Analyses of structural brain data (22 peer-reviewed papers, 577 participants) revealed highly consistent anomalies only in the basal ganglia (100% of participant groups in which this structure was examined, weighted by group sample sizes; 99.8% permutation-based likelihood the anomaly clustering was not due to chance). These anomalies were localized specifically to the anterior neostriatum (again 100% weighted proportion and 99.8% likelihood). As expected given the task dependence of activation, functional neuroimaging data (11 peer-reviewed papers, 414 participants) yielded less consistency, though anomalies again occurred primarily in the basal ganglia (79.0% and 95.1%). Multiple sensitivity analyses indicated that the patterns were robust. The meta-analyses elucidate the neuroanatomical signature of DLD, and implicate the basal ganglia in particular. The findings support the procedural circuit deficit hypothesis of DLD, have basic research and translational implications for the disorder, and advance our understanding of the neuroanatomy of language.

Assessing the knower-level framework: How reliable is the Give-a-Number task?

The Give-a-Number task has become a gold standard of children's number word comprehension in developmental psychology. Recently, researchers have begun to use the task as a predictor of other developmental milestones. This raises the question of how reliable the task is, since test-retest reliability of any measure places an upper bound on the size of reliable correlations that can be found between it and other measures. In Experiment 1, we presented 81 2- to 5-year-old children with Wynn (1992) titrated version of the Give-a-Number task twice within a single session. We found that the reliability of this version of the task was high overall, but varied importantly across different assigned knower levels, and was very low for some knower levels. In Experiment 2, we assessed the test-retest reliability of the non-titrated version of the Give-a-Number task with another group of 81 children and found a similar pattern of results. Finally, in Experiment 3, we asked whether the two versions of Give-a-Number generated different knower levels within-subjects, by testing 75 children with both tasks. Also, we asked how both tasks relate to another commonly used test of number knowledge, the "What's-On-This-Card" task. We found that overall, the titrated and non-titrated versions of Give-a-Number yielded similar knower levels, though the non-titrated version was slightly more conservative than the titrated version, which produced modestly higher knower levels. Neither was more closely related to "What's-On-This-Card" than the other. We discuss the theoretical and practical implications of these results.

Complete Genome Sequences of Four Strains from the 2015-2016 Elizabethkingia anophelis Outbreak.

The complete circularized genome sequences of selected specimens from the largest known Elizabethkingia anophelis outbreak to date are described here. Genomic rearrangements observed among the outbreak strains are discussed.

Metabolic Syndrome and Nephrolithiasis Risk: Should the Medical Management of Nephrolithiasis Include the Treatment of Metabolic Syndrome?

This article reviews the relationship between metabolic syndrome (MetS) and nephrolithiasis, as well as the clinical implications for patients with this dual diagnosis. MetS, estimated to affect 25% of adults in the United States, is associated with a fivefold increase in the risk of developing diabetes, a doubling of the risk of acquiring cardiovascular disease, and an increase in overall mortality. Defined as a syndrome, MetS is recognized clinically by numerous constitutive traits, including abdominal obesity, hypertension, dyslipidemia (elevated triglycerides, low high-density lipoprotein cholesterol), and hyperglycemia. Urologic complications of MetS include a 30% higher risk of nephrolithiasis, with an increased percentage of uric acid nephrolithiasis in the setting of hyperuricemia, hyperuricosuria, low urine pH, and low urinary volume. Current American Urological Association and European Association of Urology guidelines suggest investigating the etiology of nephrolithiasis in affected individuals; however, there is no specific goal of treating MetS as part of the medical management. Weight loss and exercise, the main lifestyle treatments of MetS, counter abdominal obesity and insulin resistance and reduce the incidence of cardiovascular events and the development of diabetes. These recommendations may offer a beneficial adjunctive treatment option for nephrolithiasis complicated by MetS. Although definitive therapeutic recommendations must await further studies, it seems both reasonable and justifiable for the urologist, as part of a multidisciplinary team, to recommend these important lifestyle changes to patients with both conditions. These recommendations should accompany the currently accepted management of nephrolithiasis.

Early postpartum pup preference is altered by gestational cocaine treatment: associations with infant cues and oxytocin expression in the MPOA.

Cross-fostering studies suggest cocaine-induced deficits in maternal behavior could be associated with altered behavior of offspring following prenatal cocaine-exposure. Neonatal vocalizations are an important offspring cue facilitating early interactions between dam and rodent pup offspring and have been shown to be altered following prenatal cocaine-exposure. It is unclear how variations in acoustic parameters of USVs impact maternal behavior and the mechanism(s) underlying these processes. The present study examined differences in cocaine-exposed and control rodent dam maternal preference of cocaine-exposed or untreated pups in a dual choice apparatus. Relationship of preference-like behavior with pup USVs and dam oxytocin expression was explored. Gestational cocaine-exposure interfered with preference-like behavior of dams on postpartum day 1 with cocaine-exposure associated with decreased time spent on the cocaine-exposed pup side compared to the control pup side, and decreases in preference-like behavior associated in part with decreased number of USVs being emitted by cocaine-exposed pups. On postpartum day 5, decreased oxytocin expression in the medial preoptic area was associated with altered preference-like behavior in cocaine-exposed dams, including frequency and latency to touch/sniff pups. Results indicate cocaine's effects on the mother-infant relationship is likely synergistic, in that cocaine influences mother and offspring both independently and concertedly and that variations within pup vocalizations and the oxytocin system may be potential mechanism(s) underlying this synergistic relationship during the postpartum period.

Retinoids induce integrin-independent lymphocyte adhesion through RAR-α nuclear receptor activity.

Oxidative metabolites of vitamin A, in particular all-trans-retinoic acid (atRA), have emerged as key factors in immunity by specifying the localization of immune cells to the gut. Although it is appreciated that isomers of retinoic acid activate the retinoic acid receptor (RAR) and retinoid X receptor (RXR) family of nuclear receptors to elicit cellular changes, the molecular details of retinoic acid action remain poorly defined in immune processes. Here we employ a battery of agonists and antagonists to delineate the specific nuclear receptors utilized by retinoids to evoke lymphocyte cell adhesion to ADAM (adisintegrin and metalloprotease) protein family members. We report that RAR agonism is sufficient to promote immune cell adhesion in both immortal and primary immune cells. Interestingly, adhesion occurs independent of integrin function, and mutant studies demonstrate that atRA-induced adhesion to ADAM members required a distinct binding interface(s) as compared to integrin recognition. Anti-inflammatory corticosteroids as well as 1,25-(OH)2D3, a vitamin D metabolite that prompts immune cell trafficking to the skin, potently inhibited the observed adhesion. Finally, our data establish that induced adhesion was specifically attributable to the RAR-α receptor isotype. The current study provides novel molecular resolution as to which nuclear receptors transduce retinoid exposure into immune cell adhesion.

9-cis-retinoic acid promotes cell adhesion through integrin dependent and independent mechanisms across immune lineages.

Retinoids are essential in the proper establishment and maintenance of immunity. Although retinoids are implicated in immune related processes, their role in immune cell adhesion has not been well established. In this study, the effect of 9-cis-retinoic acid (9-cis-RA) on human hematopoietic cell adhesion was investigated. 9-cis-RA treatment specifically induced cell adhesion of the human immune cell lines HuT-78, NB4, RPMI 8866 and U937. Due to the prominent role of integrin receptors in mediating immune cell adhesion, we sought to evaluate if cell adhesion was integrin-dependent. By employing a variety of integrin antagonist including function-blocking antibodies and EDTA, we establish that 9-cis-RA prompts immune cell adhesion through established integrin receptors in addition to a novel integrin-independent process. The novel integrin-independent adhesion required the presence of retinoid and was attenuated by treatment with synthetic corticosteroids. Finally, we demonstrate that 9-cis-RA treatment of primary murine B-cells induces ex vivo adhesion that persists in the absence of integrin function. Our study is the first to demonstrate that 9-cis-RA influences immune cell adhesion through at least two functionally distinct mechanisms.

Post-transcriptional regulation of the Ras-ERK/MAPK signaling pathway.

The Ras-ERK/MAP (Mitogen-Activated Protein) kinase signaling pathway governs many cellular processes such as proliferation, differentiation, cell fate, homeostasis, and survival in all eukaryotes. Constitutive activation of the Ras-ERK/MAPK signaling pathway often leads to promotion of abnormal cell growth and tumorigenesis. Although the regulation of the Ras-ERK/MAPK signaling pathway by post-translational modification has been well elucidated, post-transcriptional regulations of this pathway are beginning to emerge in invertebrates and this work is extended to humans. In this review, we describe the conserved regulation of Ras-ERK/MAPK signaling by RNA-binding proteins (PUF, KH-domain, HuR, and LARP) and microRNAs (let-7 family miRNAs) and important implications for human diseases including cancers.

Tips and tricks of laparoscopic partial nephrectomy.

The field of urology has embraced minimally invasive surgical procedures, from endoscopic to laparoscopic to robotic assisted surgery. As these surgical techniques are applied to renal cancer, the oncological outcomes need to be compared to more traditional open surgery. Laparoscopic partial nephrectomy emulates the open surgical technique and has become an alternative to open surgery at many academic centers. Still its wide spread adoption has been limited by the challenges of renal mass extirpation and renal reconstruction in a timely fashion to limit renal ischemia. The following review is designed to assist the urologic surgeon in performing a successful laparoscopic partial nephrectomy by detailing the "tips and tricks" of the procedure.

Notch-1 signaling is lost in prostate adenocarcinoma and promotes PTEN gene expression.

Prostate tumorigenesis is associated with loss of PTEN gene expression. We and others have recently reported that PTEN is regulated by Notch-1 signaling. Herein, we tested the hypothesis that alterations of the Notch-1 signaling pathway are present in human prostate adenocarcinoma and that Notch-1 signaling regulates PTEN gene expression in prostate cells. Prostate adenocarcinoma cases were examined by immunohistochemistry for ligand cleaved (activated) Notch-1 protein. Tumor foci exhibited little cleaved Notch-1 protein, but expression was observed in benign tissue. Both tumor and benign tissue expressed total (uncleaved) Notch-1. Reduced Hey-1 expression was seen in tumor foci but not in benign tissue, confirming loss of Notch-1 signaling in prostate adenocarcinoma. Retroviral expression of constitutively active Notch-1 in human prostate tumor cell lines resulted in increased PTEN gene expression. Incubation of prostate cell lines with the Notch-1 ligand, Delta, resulted in increased PTEN expression indicating that endogenous Notch-1 regulates PTEN gene expression. Chromatin immunoprecipitation demonstrated that CBF-1 was bound to the PTEN promoter. These data collectively indicate that defects in Notch-1 signaling may play a role in human prostate tumor formation in part via a mechanism that involves regulation of the PTEN tumor suppressor gene.

Intergenerational effects of cocaine on maternal aggressive behavior and brain oxytocin in rat dams.

Gestational cocaine treatment results in significantly increased maternal aggression towards an intruder by postpartum day six, while acute postpartum treatment dose dependently decreases maternal aggressive (MA) behavior. Both increased and decreased aggression in the cocaine-treated dams are correlated with either decreased or increased levels of oxytocin in the amygdala, respectively. The current study was an effort to determine whether the effect of gestational cocaine on maternal aggression is transient or would continue into the postpartum period; whether an intermittent cocaine treatment regimen, which incorporates gestational and postpartum intermittent cocaine treatment, would differ from chronic daily gestational treatment; and finally, whether next generation female offspring of cocaine-treated or control dams would have altered MA behavior and oxytocin system changes attributable to either prenatal drug exposure, rearing condition or both. We now report no increase in maternal aggression following chronic gestational treatment and significantly lower levels of aggression in intermittently treated dams on postpartum day eight, with no significant effects in either group on postpartum day 12. Young adult female offspring of the cocaine-treated and control dams, who reared their own natural litters and were tested on postpartum day eight for maternal aggression, had higher levels of maternal aggression towards an intruder attributable to both prenatal cocaine exposure and rearing condition. Higher aggression in cocaine-reared next generation dams was associated with lower levels of oxytocin in the amygdala. Intergenerational effects of cocaine were apparent with respect to aggression and oxytocin system changes.

Gestational ethanol and nicotine exposure: effects on maternal behavior, oxytocin, and offspring ethanol intake in the rat.

Alcohol consumption and smoking during pregnancy is common, despite the known adverse effects of these drugs on fetal development. Though studies on the effects of each drug separately are published, little is known about the effect of concurrent use of alcohol and nicotine in humans or in preclinical models. In this report, we examined the impact of continuous gestational exposure to both ethanol via liquid diet and nicotine via an osmotic minipump on maternal behavior, offspring ethanol intake, and oxytocin levels in a rat model. Dams were tested for the onset of maternal behavior with litters of unexposed surrogate pups and then killed to examine oxytocin levels within specific brain regions. Drug-exposed offspring reared by surrogate dams were tested for ethanol intake at either adolescence or adulthood, and oxytocin levels were measured in relevant brain regions after behavioral tests. Dams exhibited minor deficits in maternal care, which were associated with lower oxytocin levels in both the ventral tegmental and medial preoptic areas compared to control dams. Prenatal exposure altered sex-specific ethanol intake, with differential effects at adolescence and adulthood. Oxytocin system changes were also apparent in the ventral tegmental and medial preoptic regions of drug-exposed adolescent and adult offspring. These results suggest that dam treatment with ethanol and nicotine can somewhat negatively affect the early rearing environment, and that prenatal exposure to both of these drugs results in drinking behavior differing from what would be expected from either drug alone. Oxytocin's possible involvement in the mediation of these effects is highlighted.

Impact of gestational cocaine treatment or prenatal cocaine exposure on early postpartum oxytocin mRNA levels and receptor binding in the rat.

Prior research reported decreased oxytocin levels in specific brain regions correlated with disruptions in maternal care following gestational cocaine treatment in rats. Similarly, prenatal exposure to cocaine impaired subsequent maternal behavior in adulthood, but behavioral alterations were not associated with decreases in oxytocin levels in the same brain regions as were found in their cocaine-treated rat dams. To determine if other aspects of the oxytocin system are disrupted by cocaine treatment or prenatal exposure to cocaine during critical time points associated with maternal care, oxytocin mRNA transcription and receptor binding were examined on postpartum day two in relevant brain regions following gestational treatment with, or prenatal exposure to, either cocaine or saline. We hypothesized that oxytocin mRNA levels and receptor binding would be differentially affected by cocaine in the early postpartum period of dams and their offspring. Our findings indicate that gestational cocaine treatment resulted in significant increases in oxytocin mRNA levels in only the paraventricular nucleus of cocaine-treated dams, with almost significant increases in both generations in the supraoptic nucleus, but no significant effects of cocaine on receptor binding in either generation of dams. These findings indicate that in addition to oxytocin levels, cocaine treatment or prenatal exposure primarily affects oxytocin mRNA synthesis, with little effect on receptor binding in specific brain regions associated with maternal behavior in the early postpartum period of the rat.

CBF-1 (RBP-J kappa) binds to the PTEN promoter and regulates PTEN gene expression.

The PTEN gene regulates multiple signaling pathways that influence cell proliferation, survival and differentiation. Loss of PTEN expression is closely linked with oncogenesis. Little is known regarding regulation of PTEN gene expression. The PTEN promoter region has been reported and is regulated in part by p53. In a previous study, we found that Notch-1 signaling resulted in increased PTEN protein expression. Herein, we tested the hypothesis that the PTEN gene is a direct target of Notch-1 signal transduction, through binding of the Notch-activated transcription factor CBF-1 to the PTEN minimal promoter. 293 cells expressing constitutively active Notch-1 exhibited increased PTEN gene expression and promoter transactivation. Overexpression of CBF-1 in 293 cells resulted in decreased PTEN gene expression. Mobility shift assays and supershift assays demonstrated that CBF-1 binds to the PTEN minimal promoter. These data indicate that the Notch-1 receptor pathway is a key regulator of PTEN gene transcription.

Grade 3 ischemia on admission electrocardiogram and chest pain duration predict failure of ST-segment resolution after primary percutaneous coronary intervention for acute myocardial infarction.

OBJECTIVES: ST resolution (STR) is a surrogate marker of myocardial tissue reperfusion and a predictor of outcome after primary percutaneous coronary intervention (pPCI) for ST-elevation myocardial infarction (STEMI). Terminal QRS distortion (grade 3 ischemia) has been shown to predict failure of STR after thrombolysis for STEMI, but the ability of grade 3 ischemia to predict STR with pPCI is unclear. METHODS: We retrospectively analyzed 155 patients who underwent pPCI and compared grade 2 ischemia (ST elevation without terminal QRS distortion; n = 89) to grade 3 ischemia (n = 66) on admission for baseline characteristics, in-hospital course, and STR immediately after pPCI and at 18 to 24 hours. RESULTS: Patients with grade 3 ischemia were older (60 +/- 12 vs 56 +/- 11 years; P = .018), had more anterior STEMI (42% vs 17%; P = .0004), and were less often smokers (41% vs 90%; P = .004). The grade 3 ischemic group had significantly less complete STR (35% vs 75% [P < .00001] immediately after pPCI and 33% vs 79% [P < .00001] 18-24 hours after pPCI), a longer hospital stay (6.4 +/- 4.1 vs 4.9 +/- 1.9 days; P = .008), and higher peak CKMB (292 +/- 231 vs 195 +/- 176 ng/mL; P = .0005). Duration of symptoms before pPCI (odds ratio [OR], 0.838; 95% confidence interval [CI], 0.724-0.969; P = .017) and grade 3 ischemia (OR, 0.181; 95% CI, 0.068-0.480; P < .001) were negative predictors of complete STR, whereas nonanterior STEMI (OR, 5.95; 95% CI, 2.154-16.436; P < .001) and initial sum of ST elevation (OR, 3.132; 95% CI, 1.140-8.605; P = .027) were positive predictors. CONCLUSION: Grade 3 ischemia on presentation of STEMI and duration of chest pain are strong independent predictors of failure to achieve complete STR after pPCI.

The MLL partial tandem duplication in acute myeloid leukaemia.

Mixed lineage leukaemia gene-partial tandem duplications (MLL-PTD) characterise acute myeloid leukaemia (AML) with trisomy 11 and AML with a normal karyotype. MLL-PTD confer a worse prognosis with shortened overall and event free survival in childhood and adult AML. In spite of these clinical observations, the leukaemogenic mechanism has, so far, not been determined. This review summarises clinical studies on MLL-PTD positive AML and recent experimental findings on the putative leukaemogenic role of MLL-PTD.

Cocaine treatment alters oxytocin receptor binding but not mRNA production in postpartum rat dams.

Gestational cocaine treatment in rat dams results in decreased oxytocin (OT) levels, up-regulated oxytocin receptor (OTR) binding density and decreased receptor affinity in the whole amygdala, all concomitant with a significant increase in maternal aggression on postpartum day six. Rat dams with no gestational drug treatment that received an infusion of an OT antagonist directly into the central nucleus of the amygdala (CeA) exhibited similarly high levels of maternal aggression towards intruders. Additionally, studies indicate that decreased OT release from the hypothalamic division of the paraventricular nucleus (PVN) is coincident with heightened maternal aggression in rats. Thus, it appears that cocaine-induced alterations in OT system dynamics (levels, receptors, production, and/or release) may mediate heightened maternal aggression following cocaine treatment, but the exact mechanisms through which cocaine impacts the OT system have not yet been determined. Based on previous studies, we hypothesized that two likely mechanisms of cocaine's action would be, increased OTR binding specifically in the CeA, and decreased OT mRNA production in the PVN. Autoradiography and in situ hybridization assays were performed on targeted nuclei in brain regions of rat dams on postpartum day six, following gestational treatment twice daily with cocaine (15 mg/kg) or normal saline (1 ml/kg). We now report cocaine-induced reductions in OTR binding density in the ventromedial hypothalamus (VMH) and bed nucleus of the stria terminalis (BNST), but not the CeA. There was no significant change in OT mRNA production in the PVN following cocaine treatment.

Renal transplantation with iliac vein transposition.

UNLABELLED: We evaluated a technique for implantation of right kidneys with short renal veins without the need for venous reconstruction. METHOD: The technique of iliac vein transposition was performed in six recipients who received right kidneys with short renal veins. Two cases were living related donors, two were living unrelated, one was an autotransplant, and one was a cadaver kidney recipient. The common and external iliac veins and arteries of the recipient were thoroughly mobilized, allowing for the lateral transposition of the external iliac vein with respect to the external iliac artery. The renal vessels were subsequently implanted in an end to side fashion onto the corresponding transposed external iliac vessels. After implantation, the iliac vein remained lateral with respect to the iliac artery. CONCLUSIONS: The technique described allows for the implantation of right kidneys without the need for venous reconstruction. Such an approach is especially useful in cases of grafts with short veins.